Tornaletti S
Department of Anatomy and Cell Biology, University of Florida, Gainesville, Florida 32610, USA.
Cell Mol Life Sci. 2009 Mar;66(6):1010-20. doi: 10.1007/s00018-009-8738-x.
Arrest of transcription at sites of DNA damage represents a strong signal for apoptosis. To overcome the impasse represented by transcription complexes arrested at sites of damage, cells have evolved a specialized nucleotide excision repair (NER) pathway called transcription-coupled DNA repair (TCR), dedicated to removal of transcription-blocking lesions from the genome. This repair pathway was discovered in Phil Hanawalt's laboratory 20 years ago, but the mechanistic details are still subject of intense research. This article will review the recent literature on the subject with emphasis on how lesions affect the elongation step of transcription and how the initial steps of TCR occur in human cells. (Part of a Multi-author Review).
DNA损伤位点处转录的停滞是凋亡的强烈信号。为克服由停滞在损伤位点的转录复合物所造成的僵局,细胞进化出了一种专门的核苷酸切除修复(NER)途径,称为转录偶联DNA修复(TCR),专门用于从基因组中去除转录阻断性损伤。这条修复途径是20年前在菲尔·哈纳瓦特的实验室中发现的,但其机制细节仍是深入研究的主题。本文将综述该主题的最新文献,重点关注损伤如何影响转录的延伸步骤以及TCR的起始步骤在人类细胞中是如何发生的。(多作者综述的一部分)